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莫洛尼鼠白血病病毒gag基因P30结构域中的点突变

Point mutations in the P30 domain of the gag gene of Moloney murine leukemia virus.

作者信息

Hsu H W, Schwartzberg P, Goff S P

出版信息

Virology. 1985 Apr 15;142(1):211-4. doi: 10.1016/0042-6822(85)90435-0.

Abstract

A series of point mutations in the P30 domain of the Moloney murine leukemia virus gag gene was generated by bisulfite treatment of heteroduplex DNAs containing a single-stranded region in the gag gene. One virus bearing such a mutation exhibited a coordinate defect in gag and pol function, and was similar to previously described deletion mutants with alterations in this gene. One mutant virus displayed a different phenotype: it could assemble virion particles and provide pol function, but the particles were defective in the early stages of infection. The continued concordance of the mutants' failure or ability to both assemble virions and provide pol lends further support to the proposal that similar parts of the gag gene are required for these two processes.

摘要

通过对莫洛尼鼠白血病病毒gag基因中含有单链区域的异源双链DNA进行亚硫酸氢盐处理,在gag基因的P30结构域产生了一系列点突变。携带这种突变的一种病毒在gag和pol功能上表现出协同缺陷,并且与先前描述的该基因发生改变的缺失突变体相似。一种突变病毒表现出不同的表型:它能够组装病毒粒子并提供pol功能,但这些粒子在感染早期存在缺陷。这些突变体在组装病毒粒子和提供pol功能方面的失败或能力的持续一致性,进一步支持了gag基因的相似部分对于这两个过程是必需的这一观点。

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